Motor nerve conduction velocity and somatosensory evoked potentials in the newborn and young child in relation to thyroid function Smit, B.J.

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1 UvA-DARE (Digital Academic Repository) Motor nerve conduction velocity and somatosensory evoked potentials in the newborn and young child in relation to thyroid function Smit, B.J. Link to publication Citation for published version (APA): Smit, B. J. (1999). Motor nerve conduction velocity and somatosensory evoked potentials in the newborn and young child in relation to thyroid function General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam ( Download date: 20 Oct 2018

2 C h a p t e r l General introduction

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4 General introduction 11 General introduction Thyroid hormone is essential for normal brain development. Proliferation of axons and dendrites, synapse formation, gliogenesis and myelination are known to be regulated by thyroid hormone. 1 Thyroid hormone deficiency during brain development, as in congenital hypothyroidism, can cause problems in motor and cognitive development. 2 In addition, transient hypothyroxinemia, which is commonly found in preterm infants, is associated with an increased risk of neurodevelopmental dysfunction. 35 Maternal thyroid disease can also interfere with normal brain development. 610 Transient hypothyroxinemia of the preterm infant may be caused by immaturity of the hypothalamo-pituitary-thyroid axis, interruption of maternal-fetal transfer of thyroid hormones, sick euthyroid syndrome or a combination of these factors It is still uncertain whether transient hypothyroxinemia in preterm infants causes a shortage of thyroid hormone at the cellular level in the nervous system, as is the case in congenital hypothyroidism, and thus requires L-thyroxine supplementation Until now, six prospective studies in preterm infants have been performed to examine the effect of thyroid hormone supplementation on mortality, morbidity and neurodevelopmental outcome None of these studies provides sufficient evidence to implement thyroid supplementation in preterm infants in clinical practice. In addition to these clinical studies, more insight could be obtained by investigating the effect of hypothyroxinemia or maternal thyroid disease on the developing nervous system itself. For this purpose, neurophysiologic methods such as measuring motor nerve conduction velocities and latencies of somatosensory evoked potentials, may be used. In patients with congenital hypothyroidism prior to treatment, slow nerve conduction velocity was reported. Also in patients with congenital hypothyroidism, prolonged latencies of somatosensory evoked potentials during the first year of life were found and interpreted as a sign of a transient shortage of thyroid hormone in the nervous system For preterm infants an association between low serum thyroxine concentrations and a delay in neural maturation was reported. 34 Measuring motor nerve conduction velocities and latencies of somatosensory evoked potentials may be utilized to study the effect of transient hypothyroxinemia and maternal thyroid disease on the maturation of the developing nervous system. These measures may also be employed when studying the effect of intervention strategies such as thyroid hormone supplementation in very preterm infants.

5 12 Chapter I Scope of the thesis This thesis describes the use of motor nerve conduction velocities (MNCVs) and latencies of median nerve somatosensory evoked potentials (SEPs) in the newborn and young child in order to study the effect of thyroid function on the maturation of the developing nervous system. Literature reviews on MNCV and on median nerve SEPs are given in chapters 2 and 3, respectively. Until now, in very preterm infants insufficient reference values are available. Reference values for MNCV in ulnar and posterior tibial nerves in very preterm infants are described in chapter 4. Reference values for latencies of median nerve SEPs are described in chapter 5. In chapter 6 the neurological development of children born to mothers with known thyroid disease during pregnancy, is described. In these infants MNCVs and latencies of median nerve SEPs were measured as well. Chapter 7 describes an MNCV study of an L-thyroxine supplementation trial in a group of 200 infants born at less than 30 weeks' gestation. In chapter 8, a study of latencies of median nerve SEPs in the same L-thyroxine supplementation trial is described. The main results of the various studies and their implications are summarized in chapter 9. References 1 Porterfield SP Hendrich CE. The role of thyroid hormones in prenatal and neonatal neurological development - current perspectives. Endocrine Rev 1993;14: Kooistra L, Laane C, Vulsma T, Schellekens JMH, Van Der Meere JJ, Kalverboer AE Motor and cognitive development in children with congenital hypothyroidism: a long-term evaluation of the effects of neonatal treatment. J Pediatr 1994;124: Meijer WJ, Verloove-Vanhorick SP, Brand R, van den Brande JL. Transient hypothyroxinaemia associated with developmental delay in very preterm infants. Arch Dis Child 1992;67: Den Ouden AL, Kok JH, Verkerk PH, Brand R, Verloove-Vanhorick SR The relation between neonatal thyroxine levels and neurodevelopmental outcome at age 5 and 9 years in a national cohort of very preterm and/or very low birth weight infants. Pediatr Res 1996;39: Reuss ML, Paneth N, Pinto-Martin JA, Lorenz JM, Süsser M. The relation of transient hypothyroxinemia in preterm infants to neurologic development at two years of age. N Engl J Med 1996;334: Man EB, Serunian SA. Thyroid function in human pregnancy. IX. Development or retardation of 7-year-old progeny of hypothyroxinemic women. Am J Obstet Gynecol 1976;125: Daneman D, Howard NJ. Neonatal thyrotoxicosis: Intellectual impairment and craniosynostosis in later years. J Ped 1980;97:

6 General introduction 13 8 Cove DH, Johnston E Fetal hyperthyroidism: Experience of treatment in four siblings. Lancet 1985;l(8426): Marsuura N, Konishi J and the transient hypothyroidism study group in Japan. Transient hypothyroidism in infants born to mothers with chronic thyroiditis - A nationwide study of twenty-three cases. Endocrinol Japon 1990;37: Xue-Yi C, Xin-Min J, Zhi-Hong D, Rakeman MA, Ming-Li Z, O'Donnell K, et al. Timing of vulnerability of the brain to iodine deficiency in endemic cretinism. N Engl J Med 1994;331: Uhrmann S, Marks KH Maisels MJ, Kulin HE, Kaplan M, Utiger R. Thyroid function in the preterm infant: A longitudinal assesment. J Pediatr 1978;92: Fisher DA. Euthyroid low thyroxine and triiodothyronine states in premature and sick neonates. Ped Clin North America 1990;37: Rooman RP, Du Caju MVL, Op De Beeck L, Doex M, Van Reempts P Van Acker KJ. Low thyroxinaemia occurs in the majority of very preterm newborns. Eur J Pediatr 1996;155: Van Wassenaer AG, Kok JH, Dekker FW, de Vijlder JJM. Thyroid function in very preterm infants: Influences of gestational age and disease. Pediatric Res 1997;42: Soulioti AMA, Roomi LAI. Transient neonatal hypothyroidism in very low birthweight infants: is treatment necessary? [letter] Lancet 1985;2(8453): Weichsel ME jr. Thyroid hormone replacement therapy in the perinatal period: Neurologic considerations. J Ped 1978;92: Lucas A, Morley R, Fewtrell MS. Low triiodothyronine concentrations in preterm infants and subsequent intelligence quotient (IQ) at 8 years follow up. Br Med J 1996;312: Brook CGD. Commentary: Do preterm infants need thyroxine replacement? Br Med J 1996;312: Vulsma T, Kok JH. Prematurity-associated neurologic and developmental abnormalities and neonatal thyroid functions. N Engl J Med 1996;334: Fisher DA. Editorial: The hypothyroxinemia of prematurity. J Clin Endocrinol Metab 1997;82: Morreale de Escobar, Ares S. The hypothyroxinemia of prematurity. [letter;comment] J Clin Endocrinol Metab 1998;83: Schönberger W, Grimm W, Emmrich P Gempp W Reduction of mortality rate in premature infants by substitution of thyroid hormones. Eur J Pediatr 1981;135: Chowdhry P Scanion JW, Auerbach R, Abbassi V. Results of controlled double-blind study of thyroid replacement in very low-birth-weight premature infants with hypothyroxinemia. Pediatrics 1984;73: Eggermont E, Vanderschueren-Lodeweyckx M, De Nayer P Smeets E, Vanacker G, Cornette C, et al. The thyroid-system function in preterm infants of postmenstrual ages of 31 weeks or less: evidence for a "transient lazy thyroid system". Helv Paediatr Acta 1984;39: Amato M, Pasquier S, Carasso A, Von Muralt G. Postnatal thyroxine administration for idiopathic respiratory distress syndrome in preterm infants. Hormone Res 1988;29: Van Wassenaer AG, Kok JH, de Vijlder JJM, Briët JM, Smit BJ, Tamminga P, et al. Effects of thyroxine supplementation on neurologic development in infants born at less than 30 weeks' gestation. N Engl J Med 1997;336: Vanhole C, Aerssens P Naulaers G, Casneuf A, Devlieger H, Van den Berghe G, et al. L-thyroxine treatment of preterm newborns: clinical and endocrine effects. Ped Res 1997;42:87-92.

7 14 Chapter I 28 Moosa A, Dubowitz V. Slow nerve conduction velocity in cretins. Arch Dis Child 1971;46: Giroud M, Tenenbaum D, D'Athis P Dumas R, Nivelon JL. Neurophysiological study of peripheral nerves in newborn infants with congenital hypothyroidism. Value in the surveillance of replacement therapy. Arch Fr Pediatr 1988;45: Laureau E, Vanasse M, Hebert R, Letarte J, Glorieux J, Desjardins M, et al. Somatosensory evoked potentials and auditory brain-stem responses in congenital hypothyroidism. I. A longitudinal study before and after treatment in six infants detected in the neonatal period. Electroenceph Clin Neurophysiol 1986;64: Norcross-Nechay K, Richards GE, Cavallo A. Evoked potentials show early and delayed abnormalities in children with congenital hypothyroidism. Neuropediatr 1989;20: Bongers-Schokking CT, Colon EJ, Hoogland RA, de Groot CJ, van den Brande JL. Somatosensory evoked potentials in neonates with primary congenital hypothyroidism during the first week of therapy. Pediatr Res 1991;30: Bongers-Schokking CT, Colon EJ, Mulder PGH, Hoogland RA, de Groot CJ, van den Brande JL. Influence of treatment on the maturation of the somesthetic pathway in infants with primary congenital hypothyroidism during the first year of life. Pediatr Res 1993; 34: De Vries LS, Heckmatt JZ, Burrin JM, Dubowitz LMS, Dubowitz V Low serum thyroxine concentrations and neural maturation in preterm infants. Arch Dis Child 1986;61: